Scientists based at the Francis Crick Institute and UCL discovered more about what makes a ‘good’ versus a ‘bad’ target for immune cells to spot on cancer cells. This could have help scientists develop better ways to use immunotherapies and help them understand why these treatments don’t work for all cancers.

And our scientists are studying ways to engineer more potent cancer-fighting immune cells by using gene editing to delete their sleep function. This could stop cancer switching off attacking immune cells, but it’s still being tested in mice so it’s early days.

Results from tests looking at using immunotherapies to treat pancreatic cancer have been disappointing, but research from the Beatson Institute in Glasgow might shed some light on why this is. They found that molecules in pancreatic tumours’ surroundings were stopping the cancer-fighting immune cells attacking the tumour, and drugs that block these molecules helped boost the power of immunotherapies in mice.

Another team at the University of Cambridge focused on ovarian cancer and showed that the level of a faulty cancer gene – p53 – detectable in DNA from blood samples following treatment could be a good early indication of how well the cancer is responding.

Both of these studies are still early in development – bigger clinical trials will need to be carried out to find out if they improve the outlook for patients. But it’s a promising area of research, and one we’re keeping an eager eye on.

Scientists discover new way to tackle brain tumours

Our scientists found that a curable type of medulloblastoma brain tumours in children – called WNT medulloblastoma – grow ‘leaky’ blood vessels that allow high levels of chemotherapy drugs to reach the cancer cells and destroy them. This discovery helps scientists understand why this type of tumour respond better to treatment and could help them develop more effective treatments for other harder to treat types of medulloblastoma.

And our scientists in Edinburgh made it possible to see the unexpected relationship that specialised immune cells in the brain (called microglia) have with brain tumour cells. Their findings could open up a new way to test drugs for glioblastoma, the most common type of brain tumour.

Fewer hospital trips for men with prostate cancer

Results from a large clinical trial showed that fewer, stronger doses of radiotherapy could be just as effective in treating men with prostate cancer as more, smaller doses. This would mean fewer trips to the hospital for men, potentially fewer side effects, as well as savings for the NHS. This evidence should change the way men are given radiotherapy for prostate cancer in the UK.

Why cancer is more than just bad luck

Our researchers in Cambridge, and colleagues in the US, uncovered the ‘perfect storm’ of conditions that can lead to cancer. The discovery could help explain why some organs are more susceptible to developing tumours than others and explains why cancer is more than just bad luck.

Researchers from Cambridge also found a new and potentially better way to spot oesophageal cancer at a very early stage. Using an infra-red light and a dye that sticks to healthy oesophageal cells but not to precancerous cells, they showed that this technology can spot abnormal cells that are on their way to becoming cancerous. If removed at this stage, some cases of oesophageal cancer could be prevented.

Scientists reveal ‘genetic signatures’ left by cigarette smoke

In November a study, led by scientists at the Wellcome Trust Sanger Institute, revealed some of the details of how tobacco causes such devastation to our cells and increases the risk of cancer in different organs. Different organs in the body display different hallmarks of tobacco damage, showing that the ways tobacco harms cells are more complex than we previously thought.

Pushing ‘unstable’ pancreatic cancers over the edge

Professor Andrew Biankin found that pancreatic cancer can actually be split into four different diseases based on how damaged and chaotic the tumour’s DNA is.

The findings could be used to improve treatments, and in turn survival for the disease, something which is urgently needed.

Add-Aspirin

This year saw the launch of Add-Aspirin, the world’s largest clinical trial looking at whether taking aspirin can prevent some of the most common cancers coming back. The trial will run in the UK and in India, open in more than 100 centres across the UK and recruit 11,000 patients.

Tumour evolution

Our researchers showed that the more genetic mistakes an oesophageal tumour contains, the more aggressive it’s likely to be. They also showed that drugs like cisplatin – the standard treatment for oesophageal cancer – were less likely to work when the tumour had lots of mistakes.

In the future, the findings could allow doctors to better tailor oesophageal cancer treatment by identifying patients who are more or less likely to respond to drugs like cisplatin.

The Grand Challenge

In October we launched Grand Challenge, a £100m scheme tackling some of the biggest hurdles and challenges in understanding, preventing and treating cancer.

Understanding more about ‘double positive’ breast cancer

Cambridge-based Dr Jason Carroll and his team uncovered vital clues that might explain why women with breast cancer who have high levels of both the oestrogen and progesterone receptors (‘double-positive’) have the best chance of surviving.

They found that turning on the progesterone receptor re-programmes the effects of oestrogen on breast cancer cells, slowing down their growth. It’s early research, but it could lead to better treatments for women with ‘double positive’ breast cancer in future.

We get exciting early results from our clinical trial of Cytosponge, a simple sponge on a string test, showing that it’s just as good at detecting people who are at higher risk of developing oesophageal cancer as more invasive endoscopy procedures.

Our researchers show that a combination of two drugs is far more effective against pancreatic cancer than each one on its own – both are now being tested together in an early stage clinical trial.

A major trial funded by Cancer Research UK shows that adding chemo to radiotherapy can halve the risk of bladder cancer coming back after treatment, changing the way that people with the disease are treated.

Our scientists finally find vital DNA repair ‘scissors’ after an 18-year long hunt, revealing more about how faults in this process can lead to cancer. And at The Institute of Cancer Research, our scientists figure out the three-dimensional structure of a molecule called Hsp90, which helps to fold up proteins inside cells. This underpins the development of new cancer drugs that are now being tested in clinical trials.

Thousands of our supporters get involved in the successful campaign to bring in smoke-free legislation, which comes into effect in the UK in 2007 – a move that will prevent thousands of premature deaths over the next decade.

Our researchers help to run one of the largest ever clinical trials testing the benefits of chemotherapy for bowel cancer. The trial showed for the first time that chemotherapy could help to improve survival for people whose cancer was less advanced, and changed the way that patients are treated.

We home in on new breast and bowel cancer genes in groundbreaking studies.

Working together with the Brain Tumour Charity, our clinical trial shows that using chemotherapy to delay or avoid radiotherapy in children under three with ependymoma reduces the risk of health problems later in life.

We show that white blood cell donations could be used to treat transplant patients who develop particular cancers related to virus infection.

We show that cancers caused by faulty BRCA1 or BRCA2 genes can be killed by drugs called PARP inhibitors. These treatments are now being tested in clinical trials with promising results, and could potentially treat other types of cancer too.

We show that technique called sentinel node biopsy can reduce the side effects of breast cancer surgery. This is now the preferred way of finding out whether breast cancer has spread to the lymph nodes.

A unique 50-year study that we helped to fund shows that smokers die on average 10 years earlier than non-smokers. But stopping at any age - even in later life - cuts the risk, highlighting the importance of quitting.

Our researchers find out how a virus causes a rare type of cancer called Kaposi’s sarcoma, which tends to affect people with HIV. It was also our researchers who made the link between the virus and the cancer, back in 1990.

Our scientists discover a gene that is the ‘missing link’ between non-inherited and inherited forms of breast and ovarian cancers, helping us to understand how they develop and paving the way for future treatments.

We fund a clinical trial showing that adding chemotherapy to radiotherapy can help improve survival from medulloblastoma, the most common type of brain tumour in children.

We prove that high-dose chemotherapy is more effective than lower doses for treating multiple myeloma, a cancer of the bone marrow.

Our scientists find that faults in a gene called BRAF are involved in more than half of all cases of melanoma – the most dangerous form of skin cancer. The work has led to the rapid discovery and development of treatments designed to block BRAF, one of which – vemurafenib (Zelboraf) – is now available for patients on the NHS.

Our researchers find a molecule in urine that reveals the presence of bladder cancer. Today, their discovery is being developed into tests for prostate and bladder cancer that could help to save many lives by diagnosing the diseases earlier.

We launch the first UK trial of a vaccine against the virus that causes cervical cancer. Today, a vaccination programme has been rolled out for girls across the UK, which should save many lives in the future.

We play a vital role in setting up and leading the National Cancer Research Institute, bringing together researchers, doctors, patients and funding organisations across the UK to make faster, more co-ordinated progress in beating cancer.

We support early trials of rituximab (Mabthera) – a drug that has made a big difference to survival for people with certain types of lymphoma.

We showed that faults in a gene called BRCA2 are responsible for around one in 20 cases of prostate cancer that run in families , and track down the location of a gene called TGCT-1, linked to testicular cancer.

We figure out an important step in how damaged DNA is ‘unpackaged’ so it can be repaired. Damaged DNA is a key cause of cancer, so discovering how it is fixed, and what happens if it isn’t, is crucial to understanding how cancer starts and how to tackle it more effectively.

Our scientists uncover some of the lifestyle factors linked to HPV infection and cervical cancer, particularly smoking, having a high number of sexual partners and starting to have sex at a younger age.

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